Our work on heritable forms of cancer in man suggests than "non-tumor" cutaneous cells can be utilized for diagnosis of clinically latent manifestations of neoplasia. Abnormal phenotypic expressions have been identified in cultured skin fibroblasts (SF) derived from normal-appearing skin biopsies of tumor-prone and tumor-bearing individuals with hereditary adenomatosis of the colon and rectum (ACR). These consisted of growth disorders, increased proteolytic activity, cytoskeletal alterations, and increased susceptibility to transformation by the Kirsten murine sarcoma virus. We have proposed that the ACR cell exists in an initiated state due to a dominant mutation. Apparently, systemic disorders occurring within stromal cells of individuals at high risk of cancer are intrinsically linked to cancer and will be used in studies concerning cancer causation and cancer progression. The present report concerns: 1) the apparent susceptibility of ACR cells to an SV40-induced T-antigen display and transformation; 2) the ability of SF derived from normal and ACR individuals to repair irradiation-induced defective SV40 virus functions in infected cells; 3) the expression of neoantigens by skin fibroblasts derived from normal and ACR individual prior to and following infection by DNA and RNA oncogenic viruses; and 4) the effects of SV40 and 12-0-tetradecanoyl phorbol-13-acetate (TPA) on the phenotypic profile of ACR cells.